Dear colleagues and students:

The third seminar in the Fall 2004 Bone Seminar Series will be on
Tuesday November 16th with a presentation by Janet Rubin, Professor
of Medicine in the Division of Endocrinology and Metabolism at the
Emory School of Medicine. Janet will speak on "Turning Mechanical
Signals into Biological Effects."

Details of all seminars appear on our website:
Details of this seminar appear below.

I would greatly appreciate in any person interested in the Bone
Seminar Series, the Bone Fluid Flow Workshops or the
website, filling out a questionnaire to help me
prepare the annual report to the National Science Foundation, which
supports these activities. The questionnaire is also downloadable at

Many thanks, Steve Cowin


Speaker: Janet Rubin M.D., Professor of Medicine, Division of
Endocrinology and Metabolism, Emory University School of Medicine and
the Atlanta Veterans Affairs Medical Center, Atlanta, GA


PLACE AND TIME: Room 9207, CUNY Graduate Center
7:00 PM, November 16th, 2004

Abstract: Biophysical input generated during normal physiologic
loading is a major determinant of bone mass and morphology. Our
laboratory's interest is in how bone cells sense and transduce
signals generated during loading, and how this cellular response
leads to skeletal adaptation to its mechanical environment. We have
shown that substrate strain regulates gene expression in bone stromal
cells, decreasing expression of RANKL and increasing expression of
eNOS/nitric oxide. These changes generate a local environment that
is inhibitory for osteoclast recruitment. The ability of mechanical
strain to induce this functional response requires activation of the
ERK1/2 MAP-Kinase pathway. The proximal signaling cascade leading to
ERK1/2 activation is stunningly specific, and suggests that the
putative mechanotransducer occupies a discrete membrane location.
Our most recent work suggests that the mechanical signal arises from
events occurring within a lipid raft. Distal to ERK1/2 activation,
we will also consider possible mechanisms by which strain may inhibit
RANKL gene transcription through altering chromatin interactions with
the RANKL promoter. By defining the mechanisms involved in strain
regulation of osteoclast formation we hope to generate new paradigms
for understanding how cells convert mechanical information into
biological effects.

RESEARCH INTERESTS OF Janet Rubin: Mechanical and hormonal control
of bone remodeling, gene therapy systems, tumor metastases in bone


Questions and Feedback Contact

Stephen C. Cowin PhD
New York Center for Biomedical Engineering
Departments of Biomedical and Mechanical Engineering
School of Engineering
The City College of New York
138th Street and Convent Avenue
New York, NY 10031-9198, USA

(212) 799-7970 (Office at Home)
(212) 650-5208 (Office at Work)

(212) 799-7970 (Office at Home)


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